Sentence examples for mediating inflammatory signalling from inspiring English sources
The TLR genes remain strong candidates for susceptibility genes in RA given their crucial role in mediating inflammatory signalling.
We first demonstrated that in both unpolarized and polarized epithelial cells, CFTR is a negative regulator of NFκB mediated inflammatory signaling.
Both our in vitro (Fig 1, 2&3) and in vivo (Fig 4&5) data clearly indicate the negative correlation between CFTR cell surface levels and NFκB mediated inflammatory signaling.
Our in vitro and in vivo data clearly support the hypothesis that CFTR serves as a negative regulator of innate immunity and both CFTR channel function and its localization to lipid rafts are critical for controlling NFκB mediated inflammatory signaling (Fig 7).
Our results suggest that by focusing on common urothelial β-AR mediated inflammatory signaling pathways, reasonable pathophysiological mechanisms and potential therapeutic strategies could be developed for chronic inflammatory diseases like IC.
NFκB plays an important role in immune function and mediating inflammatory signals.
Surprisingly, while ADAM17 is required to generate secreted EGFR ligands mediating inflammatory signals in these ZZ cells, we were unable to detect a direct inhibition of ADAM17 by M α1-antitrypsin.
As a result, our data demonstrate that AMPK- α1 as an activating kinase of TAK1 has a key role in mediating inflammatory signals triggered by TLR4 and TNF- α.
We have demonstrated a novel role for increased TN-C levels in the OA joint in promoting proteoglycan loss in addition to mediating inflammatory signals, which is supported by a correlation between TN-C levels in the knee synovial fluid and proteoglycan loss from the articular cartilage in human and rat joints.
The mechanism(s) by which CFTR mediates inflammatory signaling is under debate.
Our data indicate that VCP activity is higher in the lungs (Pa-LPS induced) and liver (constitutive and CLP induced) of adult mice compared to the pediatric as an early-age-related (Fig. 2A, B and Fig. 3D) event that may contribute to the intrinsic as well as Pa-LPS/CLP mediated inflammatory signaling, NFκB activity, ER stress and apoptosis.
